Graefe's A r c h i v e

Graefe's Arch Clin Exp Ophthalmol(1982)218:20~210

for Clinical and Experimental

Ophthalmology © Springer-Verlag 1982

Indirect Choroidal Tears and Late Onset Serosanguinous Maculopathies Christopher Dean Hart* and Ruth Raistrick Department of Ophthalmology, University of Bristol, Bristol Eye Hospital, Lower Maudlin Street, Bristol BSl 2LX, England

Abstract. The retinal changes are described in four patients who acquired indirect choroidal tears and later developed serosanguinous maculopathies. Two subsequently received photocoagulation therapy and two did not. An analysis of previous cases reported in the literature with this condition, combined with our own findings, show that only patients with ruptures close to fixation have been observed to develop late onset haemorrhages and oedema at the macula. Spontaneous resolution with preservation of useful levels of visual function not infrequently occurs, and the indications for photocoagulation therapy are probably limited.

Introduction Serosanguinous disturbances involving the macula associated with neovascular tufts arising out of indirect choroidal ruptures were first described by Gass in 1970. Fuller and Gitter 1973 reported a case with such changes in which haemorrhages and oedema resolved and the neovascularisation regressed after argon laser burns had been applied to the site of a serous leak identified by fluorescein angiographic studies. It was suggested that patients who acquired indirect choroidal tears, but retained good macular function, should remain under medical supervision so that if a pre-disciform lesion appeared treatment could be instituted promptly to prevent progressive loss of central vision. Wessing 1974 and Hilton 1975 also obtained encouraging visual results in patients after treating new vessels with the argon laser but Turut and Hochart 1979, by means of repeat fluorescein angiographic studies, showed that subretinal neovascularisation arising from indirect choroidal tears frequently resolved spontaneously. The role therefore of photocoagulation in preventing disciform maculopathies and irreversible central visual loss in this condition remains unclear. In this communication, four cases of delayed onset serosanguinous maculopathy associated with indirect choroidal tears are reported two of which received photocoagulation and two did not. All had lesions of the retina or choroid solely attributable to the effects of a blunt mechanical injury to the eye. An attempt has been made to obtain a clearer picture of how the disease process naturally evolves and the role of photocoagulation in preserving central vision is discussed. * Corresponding author

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Case Reports Case 1

Male aged 34 received injuries about the face and head in March 1977 following a criminal assault (robbery with violence). Damage to the left eye and adnexia included lacerations of both the upper and lower lid, superficial corneal abrasions, traumatic mydriasis and two indirect choroidal tears, one of which ended at the macula. Fluorescein angiographic studies performed at this time showed a window-effect in the region of the choroidal tears but no leakage of dye into the retinal tissues (Fig. 1). Vision in the left eye recovered to 6/12 but in June 1977 the patient became aware of a sudden deterioration of vision. On ophthalmic examination a few days later, deep retinal haemorrhages and oedema at the macula were observed and the visual acuity could not be improved beyond 6/60. Fluorescein angiographic studies showed evidence of dye leaking out of the choroid into the

Fig. 1. Case 1. Fluorogram of left eye 1 week after trauma. Residual phase showing hyperfluorescence in region of choroidal ruptures one of which terminates at the macula. No leakage of dye is evident. Deep retinal haemorrhages have masked choroidal fluorescence on the boundaries of tears

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Fig. 2A, B. Case 1. Fluorescein angiograms left eye 3 months after trauma. A venous phase. B residual phase. A serous leak of dye is seen diffusing into the retina from the tip of the tear impinging on the macula

Case 2

Fig. 3. Case 1. Fundus photograph left eye 8 months after trauma. The retina over the part of the tear from which fluorescein dye leaked earlier has become elevated and distorted neuroretina from an area over the tear closest to the macula (Fig. 2). No treatment was instituted. The deep macular haemorrhages and oedema cleared by November 1977 but scarring in the portion of the tear where a serous leak was detected earlier, had produced a localised elevation and distortion of the retina (Fig. 3). Hyperpigmentation was present at the edges of the tear at this site outside which there was a small circular zone of hypopigmentation. Fluorescein angiographic investigations performed in 1978 showed no evidence of leakage of dye into the retina, only areas of hyperfluorescence due to decreased pigmentation around the tip of the tear were detected (Fig. 4). The visual acuity slowly recovered to 6/24 and remained at this level when the patient was last seen in June 1980.

Male aged 24 years sustained severe facial and ocular injuries following a road traffic accident in December 1976. The nature of the perforating injuries to the left eye were such that a primary enucleation was performed. The right globe remained intact but the view of the fundus was initially obscured by a vitreous haemorrhage. This rapidly cleared and two indirect choroidal tears became evident, one of which ended just inferior to the foveola. Visual acuity recovered to 6/9 but suddenly deteriorated six weeks after injury. On examination at this time visual acuity was recorded as 6/18 and a serous sanguinous maculopathy observed (Fig. 5). Fluorescein angiographic studies showed a somewhat diffuse serous leakage of dye originating from the portion of the tear closest to fixation which gradually spread into the retinal tissues. The patient was treated with Prednisolone 15 rags daily, the dose being reduced to 5 mgs daily after one month. No photocoagulation was applied. On ophthalmoscopic examination five weeks later it was noted that the deep retinal haemorrhages had largely absorbed and in the region where the serous leakage had been detected earlier, the edges of the tear showed heavy pigmentation beyond which was a circular area of hypopigmentation. The retina overlying the tear at this site was slightly elevated and distorted. Fluorescein angiographic investigations performed at the same time revealed no evidence of any leakage of dye. Four months after injury the visual acuity in the right eye had recovered to 6/9 and no oedema or haemorrhages could be seen (Fig. 6). Vision in the right eye has remained at this level since. Case 3

Male aged 19 years received a kick to the right eye in June 1976 and on ophthalmoscopic examination shortly afterwards was noted to have a vitreous haemorrhage and two choroidal tears one of which passed just temporal to the foveola. Information concerning the presence or absence of haemorrhagic detachment of the pigment epithelium involving the macula in the

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Fig. 4A, B. Case 1. Fluorescein angiograms left eye, 18 months after trauma. A venous phase. B residual phase. Immediately adjacent to the tip of the central tear is a border of hyperpigmentation outside which is an area of hypopigmentation producing a window-effect. No leakage of dye is evident

Fig. 5. Case 2. Fundus photograph right eye 6 weeks after injury showing a deep retinal haemorrhage and oedema of the macula

Fig. 6. Case 2. Fundus photograph 4 months after injury. The serosanguinous maculopathy has resolved. Around the tip of the tear is an area of hyperpigmentation outside which is an area of hypopigmentation

immediately post traumatic period was not recorded. Visual acuity only improved to 6/24 due to the development of a pigmentary maculopathy but in November 1977 the vision in the right eye suddenly deteriorated further. On examination at this time, the right visual acuity was recorded as 6/36 and a serous sanguinous maculopathy with extensive deep retinal haemorrhages detected (Fig. 7). Fluorescein angiographic studies revealed dye leaking from the choroid and diffusing into the neural layer of the retina, from a portion of a tear closest to fixation. Zenon arc photocoagulation was applied to the site of the retinal pigment epithelial disturbance located just temporal to the foveola. On ophthalmic

examination in June 1979, a number of small areas of retinal atrophy could be seen corresponding to the site where photocoagulation had been applied earlier and in addition, localised scarring beneath the retina had elevated this tissue over the portion of the tear where a serous leak had been detected previously. No haemorrhages or macular oedema were present. Fluorescein angiographic studies showed no evidence of any leakage of dye in the region of the choroidal tears but only a window-effect resulting from changes in the overlying retinal pigment epithelium. Right visual acuity was recorded as 6/18 and has remained at this level since.

209 was felt that these appearances were indicative that a disciform lesion might be developing, argon laser burns were applied to the centre of this area. Although the visual acuity immediately fell to 6/24 after treatment, this had recovered to 6/9 seven months later. No further changes in vision have been recorded since. The residual fundus changes consist of elevation overlying the portion of the tear from which fluorescein dye was noted to have leaked earlier and hypo and hyperpigmentary changes of the retinal pigment epithelium are present overlying and around this site. The macular oedema and retinal haemorrhages have cleared. Discussion

Fig. 7. Case 3. Fundus photograph right eye 17 months after injury showing a serosanguinous maculopathy with an extensive deep retinal haemorrhage. A choroidal tear has passed through the macula

Case 4 A 12 year old school boy was struck in the right eye with a hockey stick in March 1980. Fundus examination performed a short time later showed multiple indirect choroidal tears at the posterior pole one of which ended in the macula on the temporal side. Traumatic retinal oedema was also present. Visual acuity recovered to 6/9 but deteriorated suddenly at the beginning of November 1980. On examination, soon afterwards, the vision in the right eye was recorded as 6/18 and oedema and deep retinal haemorrhages were detected at the macula. Fluorescein angiographic investigations carried out on 6.11.80 showed the presence of a focal area of dye leakage through the pigment epithelium overlying the tear closest to fixation (Fig. 8). As it

The majority of patients acquiring indirect choroidal tears retain useful levels of macular function. The exceptions are those on the one hand who show little improvement of central vision following injury because of the development of a severe posttraumatic maculopathy, or individuals in whom a rupture has occurred immediately beneath the foveola, and others were vision recovers and then deteriorates, due to macular disturbances induced either by post traumatic retinal detachments or the onset of a serosanguinous retinopathy. The symptoms of late onset serosanguinous maculopathies associated with indirect choroidal ruptures following blunt non perforating injuries appear to be fairly characteristic in that a sudden reduction of vision and sometimes metamorphosia are reported by the majority of patients. All the patients described in our series, sought ophthalmic advice on their own initiative having been advised to do so should symptoms suggestive of a traumatic retinal detachment appear. Individuals with indirect choroidal tears at risk of developing delayed central serous disturbances are those in which the ruptures have occurred close to the macula. All of the cases we have been able to find reported in the literature have shown this feature and three of our patients had tears terminating at the macula and in the fourth a rupture passed through this zone. The time interval from the initial traumatic incident to the identification of a maculopathy has been recorded as early as

Fig. 8A, B. Case 4. Fluorograms right eye, 9 months after injury. A Late venous phase. B Residual phase. Numerous choroidal tears are present, a serous leak is seen closely related to a tear terminating at the macula (arrow), diffusion of dye has become widespread in the residual transit phase

210 one month after injury (Fuller and Gitter 1973), and as long as six years (Smith et al. 1974) and twenty-eight years (Wessing 1980). Most of the cases previously reported, however, developed macular changes within 18 months of trauma. In our series the onset of a serosanguinous maculopathy ranged from 6 weeks to 17 months after injury. Both Fuller and Gitter, 1973 and Hilton 1974 made the point that every one of their patients who developed a central serosanguinous disturbance was noted to have had a haemorrhagic detachment of the retinal pigment epithelium involving the macula immediately after blunt ocular trauma. In three of our cases, 1, 2, and 4 however, where the initial post traumatic fundus disturbances had been adequately recorded, no haemorrhagic ele vations of the pigment epithelium involving the macula were seen. The presence of a central haemorrhagic retinal pigment epithelial detachment immediately after injury indicates a tear close to fixation but does not appear to have additional prognostic value with regards to the subsequent evolution of a serosanguinous maculopathy. Four patients who developed haemorrhagic detachments at the macula immediately after trauma which on resolution revealed indirect choroidal ruptures and have been regularly examined by us for not less than 18 months so far show no evidence of any additional macular disturbances. Smith et al. 1974 noted that the vascular tufts arising out of indirect choroidal tears usually remained localised and appeared to be highly amenable to treatment by photocoagulation yet the eyes of two patients who did not receive any therapy nevertheless retained useful macular function. Spontaneous regression of subretinal neovascularisation, confirmed by repeat fluorescein angiographic studies was reported by Turut and Hochart 1979, who concluded that the dangers of photocoagulation to new vessels arising out of indirect choroidal ruptures had to be balanced against the natural history of the condition. Only 9 patients reported in the literature and the four in our own series were documented as having retained a useful level of central vision, somewhat arbitrarily selected by us as being a visual acuity of 6/24 or better, prior to the development of a serosanguinous maculopathy and subsequently had their visual acuities recorded after the oedema and haemorrhages cleared. Of these 7 were treated either with zenon arc or argon laser therapy and 6 were not. In the group receiving photocoagulation, 5 retained a visual acuity of 6/24 or better, in 2 the vision deteriorated to 6/60 or less because of a recurrence of sub-retinal neovascularisation (Hilton 1974; Turut and Hochart 1979). Of the 6 patients who did not have photocoagulation 4 retained a visual acuity of 6/24 or better and 2 had visual acuities which fell to 6/60 and showed no evidence of any subsequent recovery. It is clear from these findings that the indications for carrying out photocoagulation to preserve central vision are at present not clear cut and even in cases in which a severe visual loss develops as in Case 1, partial recovery of macular function may occur in the absence of any treatment. The retina overlying choroidal tears usually remains flat and retinal activity at these sites is not obviously impaired (Hart et al. 1980) but in cases that have developed serosanguinous maculopathies a localised elevation of the retina develops and

remains due to connective tissue overgrowth presumably derived from the choroid. We found difficulty in positively identifying sub-retinal new vessels in our cases since, although the choroid within the confines of a tear can be readily examined by fluorescein angiography, localised choroidal atrophy and changes in the retinal pigment epithelium over and around the rupture tend to confuse the picture. Although none of the patients reported in our series were observed to have developed neovascular tufts of the type seen in an exudative senile disciform degeneration of the macula, it would seem likely that the haemorrhages and oedema fluid had leaked from abnormal choroidal vessels and passed through defects in the choroidoretinal barrier overlying the tear itself and not at any other site. Patients with indirect choroidal tears close to fixation who retina useful levels of vision should be warned to seek medical advice if they observe any deterioration of vision but repeated examinations over an extended period of time in the absence of any symptoms are not likely to be helpful since serosanguinous maculopathies tend to occur suddenly without prior warning. We believe that it is important to carry out fluorescein angiographic studies on patients who develop serosanguinous maculopathies but if fibrovascular activity is found to be confined largely within the margins of the tear it is probable that little benefit will be achieved by carrying out photocoagulation as the oedema and haemorrhages resolve spontaneously and some degree of recovery of vision can be anticipated. If sub-retinal new vessels are detected extending beyond the boundaries of the tear towards the foveola, photocoagulation in these circumstances might have a role to play in modifying the visual outcome. Further studies are however required to confirm or refute these suggestions.

Acknowledgements'. We wish to thank Mr. J. Morgan for photographic services, Mr. D. Lyons and Mr. W. Rich for referring cases to our unit for assessment.

References

Fuller B, Gitter K (1973) Traumatic choroidal rupture with late serous detachment of the macula. Arch Opththalmol 89:345-352 Gass J (1970) Stereoscopic atlas of macular diseases. St. Louis CV Mosley Co pp 94-96 Hart J, Natsikos V, Raistrick E, Doran R (1980) Indirect choroidal tears at the posterior pole: A fluorescein angiographic and perimetric study. Brit J OphthaImol 64:59-67 Hilton G (1975) Late serosanguinous detachment of the macula after traumatic choroidal rupture. Am J OphthalmoI 79:997 1000 Smith R, Kelley J, Harbin T (1974) Late macular complications of choroidal ruptures. Am J Ophthalmol 77:650-658 Turut P, Hochart G (1979) Les membranes neovascularies dans les ruptures choroidiennes traumatique interet de la photocoagulation. Bull Soc ophtal France 11-I2:1061-1065 Wessing A (1974) Photocoagulation guided by fluorescein angiography. Shimizu K (ed) Fluorescein angiography. ISFA-Symposium Tokyo 1972 Igaku Shoin, Tokyo pp 410-415 Wessing A (1980) Exsudative Makulopathien bei Aderhautrupturen. J.F. Bergmann Verlag, Miinchen: pp 353-356 Received October 31, 1981